Obesity Hypoventilation Syndrome

Obesity Hypoventilation Syndrome

 A 66 year old man was brought by ambulance to ED after becoming acutely dyspnoeic at home, and his wife had struggled to wake him after an afternoon sleep. He had a moderate smoking history of 20 pack years and quit 20 years ago, and drank approximately 20 units of alcohol as beer per week. There were no preceding prodromal respiratory or infective symptoms reported. On examination, he was obese with a weight of 120 kg. He was snoring, which eased with a chin-lift or jaw thrust, but he would not tolerate an airway adjunct. His respiratory rate was 8 and shallow, producing SpO2 84% on high flow oxygen. He was flushed and veno-dilated peripherally, with a tachycardia of 110 bpm sinus rhythm. Most notably, he was difficult to rouse, with a GCS of 9 (E2 M5 V2). Arterial blood sampling revealed a profound hypercapnoeic respiratory acidosis with no degree of compensation. Chest X-ray showed poorly expanded lungs with bilateral basal atelectasis and prominent pulmonary vasculature. Empiric naloxone was ineffective and he was commenced on non-invasive ventilation (NIV). The working diagnosis was an acute non-infective exacerbation of previously undiagnosed chronic obstructive pulmonary disease (COPD). Treatment involved bronchodilators, steroids and bilevel pressure support non- invasive ventilation.
One hour after NIV had been established, the patient’s respiratory acidosis was worse and his clinical picture was unchanged. He was intubated then transferred to Intensive Care. CTPA ruled out significant pulmonary emboli but was suggestive of pulmonary hypertension. Ventilation was not difficult, with near normal inspiratory pressures, and his minimal wheeze resolved quickly. As his respiratory acidosis normalised, his GCS rapidly improved to the point of safe extubation after just 48 hours. Given his obesity he was extubated to non-invasive pressure support ventilation immediately. After a further 24 hours, his gas exchange began to deteriorate again. Increasing inspiratory pressure improved his tidal volumes but his intrinsic rate of breathing slowed such that his minute ventilation remained static. He eventually found a stable equilibrium using nocturnal bilevel pressure support with a high mandatory backup rate (pressure control), which maintained a normal minute ventilation. Although he developed hypercapnoea each night, this was mild and eventually compensated. With the NIV, he did not obstruct, have hypopnoeic events or desaturated overnight, which markedly improved his daytime somnolence and effort of breathing.

What are the clinical features and approaches to management of obesity hypoventilation syndrome?

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Delirium

Delirium

A patient underwent a laparotomy due to bowel perforation with peritonitis and septic shock and required ventilation for several days. He was sedated with midazolam and fentanyl. After extubation he became agitated overnight, pulled out his invasive monitoring lines and was attempting to climb out of bed.

How should his acute confusional state be managed?Read More »

Pentoxifylline in Alcoholic Hepatitis

Pentoxifylline in Alcoholic Hepatitis

A 28 year old male presented to the Emergency Department with an upper gastrointestinal bleed. This was managed  with resuscitation and endoscopic diathermy and adrenaline injection This was his first presentation to secondary care with complications from his significant alcohol intake. He reported drinking at least 50 units of alcohol per week. Ultrasound examination demonstrated an enlarged liver with changes consistent with steatosis. On day 3 of his admission, he became tachycardic, tachypnoeic and increasingly lethargic. Examination revealed jaundice, bi-basal lung crepitations and mild confusion. Investigation confirmed an acute hepatitis by blood chemistry and repeat ultrasound. In the absence of any other cause, a diagnosis of acute alcoholic hepatitis was considered.

In patients with acute alcoholic hepatitis, does pentoxifylline reduce mortality?Read More »

Massive Pulmonary Embolism

Massive Pulmonary Embolism

A 48 year old lady was admitted to critical care whilst suffering from sepsis secondary to severe cellulitis of her leg. She was obese with a BMI of 38 and was managed with insulin and oral anti-hyperglycaemics for type 2 diabetes mellitus. A doppler scan was unable to exclude a DVT. She had a further deterioration 30 hours later. Her sinus tachycardia accelerated to 130 bpm, along with a drop in blood pressure to 100/40. Arterial blood gas demonstrated an increasing A-a gradient as his FiO2 increased. Although such changes can occur in sepsis, the acute onset led to concerns regarding venous thromboembolism and pulmonary emboli.

What are the options for prevention of venous thromboembolism and pulmonary embolism?
Transfusion in Sepsis

Transfusion in Sepsis

A 85 year old man presented with acute bowel obstruction. He had a history of hypertension and diverticulitis disease, but was active for his age. He was not known to have coronary or any other vascular pathology. At laparotomy, a large diverticulitis abscess was identified. When this was manipulated, he developed an SVT with a ventricular rate of 210 bpm which progressed to VT. He received 1 mg adrenaline and 2 minutes CPR in total, with no electrical shocks. At this point perfusion and pressure returned. Surgery was expedited and simplified. He remained intubated and ventilated on ITU post-operatively. ECG demonstrated global t-wave inversion. He required noradrenaline and adrenaline to maintain blood pressure. During the initial 48 hours, his haemoglobin (Hb) fell from 11.9 g/dl to 8.1 g/dl, raising the suggestion of packed red cell (PRC) transfusion.

What is the most appropriate threshold to transfuse packed red cells in critically ill patients?Read More »

Tranexamic Acid in Trauma

Tranexamic Acid in Trauma

A 19 year old man experienced a head on collision as the driver of a car. He suffered significant lower limb open fractures, pelvic fractures, lung injuries and a small subarachnoid bleed. Initial management was performed in ED and included oxygen, IV access and fluid, lower limb and spine immobilisation, and analgesia. He underwent a trauma series CT scan, which identified the various injuries given above. At no point was his level of consciousness a concern, and he maintained his own patent airway throughout. He did not show signs of haemodynamic instability or evidence of life threatening haemorrhage. Tranexamic acid (TXA) was not given.

What is the evidence for using tranexamic acid in trauma?

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Loop Diuretics in Acute Kidney Injury

Loop Diuretics in Acute Kidney Injury

A 65 year old woman underwent an elective mitral valve repair (MVR) and four vessel coronary artery bypass graft (CABG) procedure. Pre-operatively she was diagnosed with chronic kidney disease (CKD) secondary to hypertensive nephropathy, and chronic airway disease secondary to smoking. Her baseline creatinine was 275. Surgery was uneventful but in the post-operatively period she developed pulmonary oedema and worsening acute kidney injury (AKI). On day 2 her creatinine reached 420 and oliguria occurred (urine output < 0.5 ml kg-1 hr-1). Non-invasive respiratory ventilation provided adequate support and maintained a normal blood PaCO2 and pH, although her base excess drifted to -7 mmol l-1.Dopamine was administered at 2–10 μg kg-1 min-1, titrated to MAP ≧ 75 mmHg; pericardial pacing continued to maintain sinus rhythm at 60 bpm; her CVP was 14 mmHg and stable. Furosemide was started and given by a continuous infusion of 10 mg hr-1 after an initial bolus of 100 mg to try and help with diuresis.

Is there any evidence to support the use of loop diuretics in acute kidney injury?

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